In diffuse lung injury, optimal oxygenation occurs with high-frequency oscillatory ventilation (HFO-A, where A is active expiratory phase) when sustained inflations (SI) are applied periodically to recruit lung volume. Theoretically pulsed pressures may be safer and more effective than static pressures for reexpanding alveoli. We compared the increases in lung volume and arterial PO2 (PaO2) induced by 30-s increases in mean airway pressure in six New Zealand White rabbits made atelectasis prone by saline lavage plus 1 h of conventional ventilation. Pulsatile SI's (HFO-A left on during increase in mean pressure) of delta PSI = 5, 10, and 15 cmH2O and static SI's (HFO-A off during SI) of delta PSI = 5, 10, 15, and 20 cmH2O were delivered in random order. Lungs were ventilated at 15 Hz, inspired fractional concentration of O2 = 1.0, and mean airway pressure 15-20 cmH2O between test periods and deflated to functional residual capacity before each SI to standardize volume history. With both maneuvers, increases in lung volume and PaO2 induced by SI's were proportional to the magnitude of the SI (P less than 0.001) in all cases. Pulsatile SI's consistently increased lung volume and PaO2 more than static SI's having the same delta PSI (P less than 0.005) such that any given target PaO2 or change in volume (delta V) was achieved at 5 cmH2O less mean pressure with the pulsatile maneuver. Respiratory system compliance increased after both types of SI. Oxygenation and lung volume changes at 5 min were related with r = 0.58 (P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

An organized clinical and educational protocol to initiate ECPR for patients with OHCA is feasible and significantly reduces the key benchmark of time-to-ECPR flows.

We monitored the steady-state ventilatory responses of anesthetized cats to increases in lung volume produced by expiratory threshold loads (ETL) to study the roles of peripheral and central neural mechanisms in controlling respiration at elevated lung volumes. Application of an ETL of 5 cmH2O produced a significant decrease in respiratory frequency (-18%) but no change in minute ventilation (VE) due to a significant increase in tidal volume (VT) (19.3%). The drop in frequency was due solely to an increase in expiratory duration. ETL of 10 cmH2O significantly reduced VE (-17.5%) for the same reason. VT was maintained or increased at elevated lung volumes due to both an increase in the rate of rise of phrenic activity and a maintenance of inspiratory duration (TI) despite increases in both chemical drive and pulmonary stretch receptor (PSR) activity. No PSR adapted completely to the maintained change in lung volume. The sensitivity of the inspiratory off-switch mechanism to increases in lung volume, given by the reciprocal of the VT-TI relationship, decreased significantly during breathing on ETL. The results are consistent with the hypothesis that central habituation, not just peripheral adaptation of PSR, determines breathing pattern at elevated lung volumes.

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